1. M.A.ZOHAL pulmonologist
COPD

2. Definition
A disease state characterized by airflow limitation that is not fully reversible
Conditions include:
Emphysema: anatomically defined condition characterized by destruction and enlargement of the lung alveoli
Chronic bronchitis: clinically defined condition with chronic cough and phlegm
Small-airways disease: condition in which small bronchioles are narrowed

3. Epidemiology COPD is the third leading cause of death
COPD is the fifth leading cause of years lived with disability
affects >10 million persons in the United States.
6.8% of general population Sex
Higher prevalence in men, probably secondary to smoking
Prevalence of COLD among women is increasing as the gender gap in smoking rates has diminished.
Age
Higher prevalence with increasing age
Dose–response relationship between cigarette smoking intensity and decreased pulmonary function

14. PATHOPHYSIOLOGY of COPD chronic bronchtis
Mucus gland hypertrophy
Hyperplasia of goblet cells
Neutrophilic inflammatory reaction
Intraluminal mucus plugging
Hypertrophy of airway smooth muscle
Fibrosis of small respiratory bronchioles

15. PATHOLOGY OF EMPHYSEMA
Centrilobular In cigarette smoking and predominantly affects the upper lung zones
Centriacinar In the respiratory bronchiole,lower lung zones, higher degree of inflammation ,with AAT deficiency
Paraseptal Mainly alveolar ducts, and sacs, parenchymal fibrous stranding ,bullae formation

16. PATHOPHYSIOLOGY of COPD (emphysema )
Decreases in elastic recoil
Increases in dynamic airway compression
Fixed increase in airflow resistance
Destruction of alveolar septae

18. Risk Factors Smoking Airway hyperresponsiveness Respiratory infections
Cigarette smoking is a major risk factor.
Cigar and pipe smoking
Evidence less compelling; likely related to lower dose of inhaled tobacco by-products
Passive (secondhand) smoking
Associated with reductions in pulmonary function
Its status as a risk factor for COLD remains uncertain.
Airway hyperresponsiveness
Respiratory infections
Risk factor for exacerbations
The association of adult and childhood respiratory infections with development and progression of COLD remains unproven.

19. Risk factors
Occupational exposures to dust and fumes (coal mining, gold mining and cotton textile dust)
The magnitude of these effects appears substantially less important than the effect of cigarette smoking.
Ambient air pollution
The relationship of air pollution to COPD remains unproven.
Genetic factors
α1 antitrypsin (α1AT) deficiency

20. SMOKING AND THE NATURAL HISTORY OF COPD
Tobacco smoking accounts for 80% to 90% of the risk for COPD
There is poorer lung function and a more rapid decline in FEV 1 in smokers
Cough, sputum production, and dyspnea are much more common in smokers
Deaths ascribed to COPD are much more common in smokers

21. SMOKING AND THE NATURAL HISTORY OF COPD
The likelihood of COPD increases with:
The number of cigarettes smoked per day
The cumulative pack-years of exposure
When smoking is started at an earlier age
Low-tar, filtered cigarettes are with less symptoms than unfiltered brands, but the effects on lung function do not differ

22. SMOKING AND THE NATURAL HISTORY OF COPD
FEV 1 declines
In the average nonsmoker =30 ml/yr
In the average smoker =60 ml/yr
In sensitive (15% to 20%) smoker =100ml/yr

24. Summary Statement
There is a direct relation between the number of cigarettes smoked and the development of COPD in susceptible individuals
Pulmonary function is lost at a faster rate in smokers than in nonsmokers. In most people with COPD, symptoms develop in the fifth or sixth decade of life when the FEV 1 falls below 1.0–1.5 L
At some point after smoking cessation, pulmonary function begins to fall at a rate approximating that of the nonsmoking population

25. RISK FACTORS FOR COPD Host-Related Environmental
Airway hyperresponsiveness
Cigarette smoking
Genetic factors (poorly characterized) Severe hereditary α1 antitrypsin deficiency
Indoor air pollution from biomass fuel use in setting of inadequate ventilation Occupational dusts and chemicals
Low birth weight Maternal cigarette smoking during gestation
History of severe childhood respiratory infection Pipe/cigar smoking
HIV infection Outdoor air pollution Low socioeconomic status Intravenous drug use methylphenidate, methadone, talc granulomatosis

26. Symptoms & Signs 3 most common Additional signs and symptoms Cough
Sputum production
Exertional dyspnea, frequently of long duration
Additional signs and symptoms
Dyspnea at rest
Prolonged expiratory phase and/or expiratory wheezing on lung examination
Decreased breath sounds
Barrel chest
Large lung volumes and poor diaphragmatic excursion, as assessed by percussion
Use of accessory muscles of respiration
Pursed lip breathing (predominantly emphysema)
Characteristic "tripod" sitting position to facilitate the actions of the sternocleidomastoid, scalene, and intercostal muscles
Cyanosis, visible in lips and nail beds
Systemic wasting
Significant weight loss
Bitemporal wasting
Diffuse loss of subcutaneous adipose tissue

29. SYMPTOM & SIGN Paradoxical respiration
Inward movement of the rib cage with inspiration (Hoover's sign) in some patients
"Pink puffers" are patients with predominant emphysema—no cyanosis or edema, with decreased breath sounds.
"Blue bloaters" are patients with predominant bronchitis—cyanosis and edema.
Most patients have elements of each.
Advanced disease: signs of cor pulmonale
Elevated jugular venous distention
Right ventricular heave
Third heart sound
Hepatic congestion
Ascites
Peripheral edema

30. Diagnostic Approach Initial assessment
History and physical examination (see Signs & Symptoms)
Pulmonary function testing to assess airflow obstruction
Radiographic studies

31. Imaging Chest radiography Chest CT
Emphysema: obvious bullae, paucity of parenchymal markings, or hyperlucency
Hyperinflation: increased lung volumes, flattening of diaphragm
Does not indicate chronicity of changes
Chest CT
Definitive test for establishing the diagnosis of emphysema, but not necessary to make the diagnosis

32. Pulmonary function tests/spirometry
Chronically reduced ratio of FEV1 to forced vital capacity (FVC)
In contrast to asthma, the reduced FEV1 in COLD seldom shows large responses (>30%) to inhaled bronchodilators, although improvements up to 15% are common.
Reduction in forced expiratory flow rates
Increases in residual volume
Increases in ratio of residual volume to total lung capacity
Increased total lung capacity (late in the disease)
Diffusion capacity may be decreased in patients with emphysema.

33. Treatment Approach General
Institute therapy after assessment of symptoms, potential risks, costs, and benefits.
Only 3 interventions have been demonstrated to influence the natural history.
Smoking cessation
Oxygen therapy in chronically hypoxemic patients
Lung Volume Reduction Surgery (LVRS)
All other current therapies are directed at improving symptoms and decreasing frequency and severity of exacerbations.
Therapeutic response should determine continuation of treatment.

34. Phamacoloigical therapies
Anticholinergic drugs ( ipratropium or tiotropium )
SABA
LABA
Theophyline

35. Stable-phase COPD, nonpharmacologic therapies
Smoking cessation
General medical care
Annual influenza vaccine
Polyvalent pneumococcal vaccine is recommended.
Pulmonary rehabilitation
Improves health-related quality of life, dyspnea, and exercise capacity
Rates of hospitalization are reduced over 6 to 12 months.

36. Exacerbation
Assess the severity of both the acute and chronic components of the patient's illness.
Attempt to identify and treat the precipitant of the exacerbation.

37. Lung volume reduction surgery
Produces symptomatic and functional benefit in selected patients
Emphysema
Predominant upper lobe involvement
Contraindications
Significant pleural disease
pulmonary artery systolic pressure > 45 mm Hg
Extreme deconditioning
Congestive heart failure
Other severe comorbid conditions
FEV1 < 20% of predicted and diffusely distributed emphysema on CT or diffusing capacity for CO < 20% of predicted (due to increased mortality)

38. Lung transplantation
COPD is currently the second leading indication for lung transplantation
Candidates
≤65 years
Severe disability despite maximal medical therapy
No comorbid conditions, such as liver, renal, or cardiac disease
Anatomic distribution of emphysema and presence of pulmonary hypertension are not contraindications.

39. Prevention Smoking prevention or cessation Prevention of exacerbations
azithromycin administered daily to subjects with a history of exacerbation in the past 6 months demonstrated a reduced exacerbation frequency
Inhalation glucocorticoids should be considered in patients with frequent exacerbations or in patients with an asthmatic component.
Vaccination against influenza and pneumococcal infection

40. Median survival for severe disease (FEV1 < 1 L) is 4 years.
Prognosis
The principal determinant of morbidity in COPD is the degree of airway obstruction.
Patients who continue to smoke cigarettes experience a yearly decrease in FEV1 of 80–100 mL.
Even for patients who quit smoking, the FEV1 decreases by 30 mL per year.
Median survival for severe disease (FEV1 < 1 L) is 4 years.